Interestingly, infection with both viruses markedly promoted the expression of TLR1 and TLR2, which are sensors of bacterial components [29,30], which may be explained by the up-regulation of IFNα and IFNγ that could enhance the expression of TLR1, TLR2, TLR3, and TLR7 in viral infections [31]. The gene discussed is TLR3; the disease is viral infectious disease.